you won't find any good trials for either. there are infinitely too many variables in the horrible shape the human body is in now, and there is a lack of funding and backing for such trials. you have to rely on biology for this.

i have found several on rats where thermogenesis was impaired in some way and they gained significant weight on a high fat chow diet, but it's not the same thing.

The "metabolic advantage" was coined by Robert Atkins to sell a fad diet, he claimed you peed out up to 600 calories a day through ketones. It had and still does have hundreds of thousands of people around the world fruitlessly peeing on ketostix hoping for a purple color thinking it means they pissed out half the calories from the low carb chocolate cheesecake they just devoured.

If you really were peeing away half of your last meals calories I certainly wouldn't call it an "advantage".

There probably is an advantage to carb refeeds for a dieter, as directly after the meal it's going to be less efficient at converting it to fat and it will help increase the metabolism slightly and signal to the body that it's not starving.

Law of diminishing returns. Eating a protein content so high that carbohydrate content isn't enough would require the body to burn protein - conversion of amino acids into glucose. This is done primarily by cortisol, so the constant state of gluconeogenesis would overtime become an extremely stressful environment. I would predict a crushed libido, no energy and strong hypothyroidism. High protein =/= all protein as protein is not an efficient energy source, unlike fat and carbohydrate.

I don't suppose enjoining you to deploy your Wikipedia skills towards researching metabolism and or biochemistry would serve much of a purpose?

Ok, well, no matter, let me try to give you the Cliff's notes of Cliff's notes version about how energy metabolism works:

The fundamental driver of metabolism is the concentration gradient, you metabolise that which is most prevalent or common, meaning that if you are eating predimantly carbohydrates, that's your energy substrate. Fats, then FFAs it is, and much the same with protein. If you've ever used a blood glucose meter, then you've directly measured the concentration of glucose in your blood, which is why the units of such measurements are mmol/l in Europe. This is the scientific unit for concentration (molarity). North Americans are saddled with a non-standard unit of mg/dL.

Unlike what you seem to believe, the body is in a constant state of gluconeogenesis. As in every second of every day of your life. Several tissues like red blood cells and the kidney medula are obligate glycolytic tissues. Lacking mitochondria, they are incapable of oxidative respiration and so can only derive energy from glycolysis. The interesting thing about this is that the end product of glycolysis in the absence of mitochondria ( or sufficient oxygen in those cells possessing mitochondria ) is lactic acid. So, of course, all of us are keeling over from extreme lactic acidosis as the lactic acid builds up in our systems catastrophically altering the pH of our bodies, right? Well, no, because lactic acid is a very nice 3 carbon chain that when combined with another such molecule in hepatocytes is used as a gluconeogenesis substrate to regenerate glucose. So, if you possess red blood cells or kidneys, guess what, you are in a constant state of gluconeogenesis.

If you are eating large quantities of protein, then we can expect that your plasma will contain large quantities of amino acids. This is, after all, the point of digestion. According to you, then, in an environment replete with amino acids, metabolism would respond by secreting increased cortisol to produce yet more amino acids?? Even if you know absolutely nothing about metabolism, this makes absolutely no sense. I suspect that you threw cortisol bogeyman in there in an attempt to motivate readers to your point of view with fear and uncertainty. In any event, due to the increased concentration gradient of amino acids, this alone results in increased gluconeogenesis ( tada, back to #1 )

Below is the generic structure of an amino acid. The interesting bit there is the nitrogen, or amine, group ( the purple atom in the diagram ). What do you suppose we are left with, chemically speaking, if we were to remove the amine group ( deamination )? Give yourself three gold stars if you said a fatty acid. So, metabolically speaking, a deaminated amino acid pretty much goes through the same metabolic pathways as would a free fatty acid. The complication is the amine group. Amine groups are removed via the process of hydrolysis, which means that a water molecule is basically striped down to one hydrogen, and a hydroxy ( OH ) group. The one hydrogen atom goes to the amine group which results in ammonia being produced. Ammonia is a neurotoxin similar to arsenic in its effects which must be eliminated. The elimination of toxic amine groups is the whole purpose of the urea cycle. It is this process of metabolising free amine groups that is largely responsible for the lower energy yield of protein.

Protein poisoning is a real possibility, but has nothing to do with cortisol, per se. Rather, it comes from forcing the liver to excessively deaminate proteins and the kidneys to process excess amounts of urea. The conclusion from all of this is that protein should primarily be a structural, not energetic substrate. That is, use your protein to build your tissues, and either carbohydrates or fats for energy. Note that either fat or carbohydrate will ameliorate protein poisoning, something that doesn't seem to sit well with carbohydrate apologists, particularly when you couple that with the observation that there are essential fatty acids that must be provided by the diet, unlike the case for carbohydrates.

I will give you this much, Choco: I will agree with you that overeating protein is a bad thing. The tricky bit, of course, comes from that seemingly innocuous "overating" part.

Comments: they split 12 women into two groups of 6. Half were given a 1000-calorie low-carb diet, the other half a 1000-calorie high-carb diet. The metabolic rate of the low-carbers declined by 12.4%, the metabolic rate of the high-carbers declined by 20.8%.

It wasn't a 1000 calorie diet. Not sure how much of this I'm allowed to share...

During the 28 day treatment period, both groups consumed a daily liquid diet consisting of 530 kcal. The base diet for both groups consisted of 330 kcal as a liquid formula preparation (Cambridge Diet). This diet contained 33 gm protein, 44 gm carbohydrate, and 3 gm fat. Each diet was increased with a daily addition of 200 kcal as either carbohydrate (Polycose, Ross Laboratories, Columbus Ohio) or fat (Microlipid, Biosearch, Sommerville, NJ). Thus, the final composition of the diets were 33% and 71% carbohydrate for the LC and HC groups, respectively. Both treatment groups participated in the same exercise program consisting of jogging or brisk walking, depending on initial fitness level, to achieve a heart rate corresponding to 60% VG, max for 30 to 45 minutes. The exercise sessions took place three times per week at noon and were supervised by the experimenters. At the end of the treatment period, the participants were instructed to follow a 1,000 kcal diet of solid foods using the diabetic exchange system (20% protein, 45% carbohydrate, 35% fat) for one week post-VLCD. The exercise sessions were continued during this post-VLCD period.

If you look at the right side of the table, RMR (kcal/d/kg), the LC advantage is lost. Why? From the discussion:

A decrease in RMR may be secondary to a decrease in lean body mass since it has been shown that RMR is highly correlated with the fat free mass.4*2’ The fact that RMR, when expressed per body weight, was no longer significantly altered over time by the VLCDs supports the concept that the drop in RMR during caloric restriction coincides with a decrease in body weight.

Edit: The HC group weighed less on average. (My mistake, got mixed up) A 530 calorie diet doesn't seem to be the best context in which to discuss thermogenesis.

@Timthetaco..... Those were a couple of examples of the type of studies I would like to see, not necessarily proof of a position in and of themselves. I understand (as zach pointed out) that these studies have issues.

Just to make it clear, I am not arguing FOR the existence of a metabolic advantage in low carb or ketogenic dieting. I am asking for the evidence to the exact contrary. A popular meme as of late is that carbohydrates increase our metabolism. I was asking if there was human trials that support that claim. If in fact a higher proportion of carbs in isocaloric diets increase our metabolic rate then it should be measurable right?

Here is a newer study that most round here are now familiar with and its a bit better in terms of methodology:

Conclusion Among overweight and obese young adults compared with pre–weight-loss energy expenditure, isocaloric feeding following 10% to 15% weight loss resulted in decreases in REE and TEE that were greatest with the low-fat diet, intermediate with the low–glycemic index diet, and least with the very low-carbohydrate diet.

You probably recognize that I'm simply putting the onus of the "metabolic advantage" back on the high carb diet, since this..... "well its the thermogenic effect of food.... you can't argue"..... sort of mentality is beginning to take hold. I thought it was worth exploring the human trials to see how it held up to scrutiny.

I'm not trying to be a prick about it. There are surely plenty of reasons to change your macronutrient profile. I'm just not convinced that.... "because carbs have a greater thermogenic effect" is a good one. You know its kind of funny cause its the exact same thing that forgotmylastusername talks about in reverse. Some people in ketosis think you cant gain fat as long as you are peeing it out, and it seems some people eating high carb low fat think they cant gain fat cause they will just burn it all up as heat energy. I don't actually believe in either of those myself

The biggest metabolic advantage I can think of is;
Carbs elicit an anabolic response from the body, Fats elicit a catabolic response. Proteins elicit a neutral response.

I'm sorry, but where do you get this notion from? Carbs are anabolic in what sense? Perhaps to the extent that eating carbs prevents protein oxidation, but otherwise, the only thing that is anabolic is protein. You cannot build proteinaceous tissues with carbs. Period.

Originally Posted by dilberryhoundog

For a while after eating carbs it is difficult for the body to remove energy from storage cells. To liberate fat and glucose the body needs glucagon. Carbs turn off glucagon. Someone that predominately ate carbs all day, then switched to low carb, will probably see a large metabolic advantage effect.

Trafficking of free fatty acids is predominantly influenced by insulin, not glucagon. Eating continuously ( "all day" ) effectively elevates insulin continuously, irrespective of carbohydrate content. It does not take a large increase in circulating insulin in order to elicit a large reduction in lypolysis. Beef elicits a significant insulin response, so, if you switched to eating mostly meat, your "large metabolic advantage" is moot.

Originally Posted by dilberryhoundog

It is not the calories, all calories are basically equal, it is the body's different response to different macros.

Ok, one sentence, one contradiction. How can you affirm that the body has different responses to macros, but maintain that all calories are "basically equal"? Either the body responds differently to fat vs. carbs, for instance, meaning that 100 calories of fat will not be same as 100 calories of carbs due to this difference, or, the body responds in the same fashion to carbs vs. fats meaning that 100 calories of fat are, near as makes no difference, equivalent to 100 calories of carbs. Right or wrong, pick one, and try to stick with it.

No. I am making a prediction - you will not provide one single study - anywhere - that shows a skin disease caused by a deficiency in polyunsaturated fat. Any study that attempts to draw that conclusion has confounding factors galore. That is my stance - I challenge you to prove ONE.

There is no such thing as an "essential fatty acid." Your body does not need omega 3 and omega 6. There is no study ANYWHERE that has shown "essential fatty acids" to be actually essential. Do you understand this? This is marketing speak from 40 years ago and holds no basis in reality. The body explicitly does not manufacture polyunsaturated fat because it is inherently toxic to the body in significant quantities. Your body does not want PUFA in it.

Ok, I'll bite. Shockingly, it turns out Choco doesn't really know what he's talking about. So where did this EFA propaganda come from? The seminal paper was from 1929 entitled "A NEW DEFICIENCY DISEASE PRODUCED BY THE RIGID EXCLUSION OF FAT FROM THE DIET.*" which fed experimental rats a diet completely devoid of fat. How did the animals fare under this regime?

Originally Posted by A NEW DEFICIENCY DISEASE PRODUCED BY THE RIGID EXCLUSION OF FAT FROM THE DIET.

an abnormal, scaly condition of the skin is observed between the 70th and the 90th day of life. Later the tip of the tail may become inflamed and swollen, and the whole tail soon is heavily scaled and ridged. Hemorhagic spots may arise in the skin throughout the entire length of the tail. The swelling of the tip may gradually be replaced by a true necrosis, resulting in the loss of 1 to 3 cm. of the tail. The hind feet become red and somewhat swollen at times, in some cases with large scales over the dorsal surfaces. The hair on the back of the body becomes filled with dandruff. There is a tendency to lose the hair, especially about the face, back, and throat. Sores often appear on the skin.

The pathology here is really interesting, particularly with respect to Choco's claim that fatty acid deficiencies do not manifest in any way as skin conditions, which, at least for rats, is completely wrong, and we've known about it for almost a century now.

Originally Posted by ChocoTaco369

Cod liver oil is poisonous and you're giving it to your child. I would continue your research.

When the seed and fish oil industry was going under decades ago because the drying oils they were selling to the paint industry got replaced with cheap petroleum-based products, the seed oil industry came out of the hole pretty quickly with the war on saturated fats and cholesterol. Margarine was born! It was a much more difficult hill for fish oil manufacturers to climb because fish oil contains a lot of cholesterol, but it has finally made it into the "health food" market over the past decade. I find it funny that you wholeheartedly acknowledge that soybean oil is really bad for you, but you can't seem to understand that fish oil is bad for you for the exact same reason. I don't know who fabricated this "omega 3 : omega 6 ratio" myth, but it's a pretty incredible lie given there is nothing backing it up other than hearsay. You are giving your child WD40 pills. SMH.

Choco's train of thought goes completely off the rails here equating margarine with essential fatty oils. So, in Choco's febrile imagination, partially hydrogenated vegetable oil is exactly the same as fish oil and WD40. Only someone with no understanding of biochemistry would make such a ridiculous claim. Speaking of fish oils, take a look at the below study which, among other things outlines some of the symptoms of essential fatty acid deficiency (EFAD) in humans (i.e. dermatitis and growth retardation ), as well as how to remedy that :

Originally Posted by The essentiality of arachidonic acid and docosahexaenoic acid

The purpose of this review is to correlate the clinical finding that patients receiving parenteral nutrition with a fish oil-based lipid emulsion do not develop essential fatty acid deficiency (EFAD) with an experimental murine model, thus showing that arachidonic acid (AA) and docosahexaenoic acid (DHA) are likely to be the essential fatty acids...No patients receiving parenteral nutrition with a fish oil-based lipid emulsion in our institution have developed biochemical or clinical evidence of EFAD such as an elevated triene-tetraene ratio, growth retardation or dermatitis. This observation parallels our previously published animal studies, which demonstrated prevention of EFAD when thirteen percent of total calories were from fish oil. Moreover, current work in our laboratory shows that AA and DHA provision alone is sufficient to prevent biochemical and physiologic evidence of EFAD in a murine model.

So what happens when we feed rats fat, but not the essential fatty acids that Choco doesn't believe in?

Originally Posted by Effect of dietary linoleic acid and essential fatty acid deficiency on resting metabolism, nonshivering thermogenesis and brown adipose tissue in the rat.

Rats were fed a diet either deficient (0.05%) in essential fatty acids (EFA), or providing 4% (control) and 10% (surplus) of the total energy intake in the form of linoleic acid. All diets were isoenergetic and provided 13.9% of the energy as fat. The rats were kept at 29 or 5 degrees C. Growth and food intake of rats fed linoleic acid surplus at either temperature for 10 wk were not different from that of controls; basal metabolism, norepinephrine-induced nonshivering thermogenesis (NST) and thermogenic variables in the brown adipose tissue (amount of mitochondria and mitochondrial uncoupling protein) also were not different. The effects of EFA deficiency were drastically enhanced in the cold: After 10 wk of consuming a diet low in EFA at 5 degrees C, the body weight of rats was 75% of that of controls (87% at 29 degrees C); the food intake was 135% of controls at 5 degrees C (120% at 29 degrees C). The resting respiration in deficient rats was 125% of controls at 5 degrees C (110% at 29 degrees C); body temperatures as low as 35.1 degrees C were measured in deficient rats after 3 wk at 5 degrees C; the cold tolerance of the rats was significantly diminished (30% died within 3 wk at 5 degrees C), thus emphasizing the essential role of dietary EFA during cold stress.

Well, we certainly observe a difference, and the rats that are not fed essential fatty acids do worse with respect to growth and cold tolerance.

Back to humans, note the bit in bold again, yeah, it's going to address skin changes among other things:

Originally Posted by The possible role of essential fatty acids in the pathophysiology of malnutrition: a review

Biochemical evidence of essential fatty acid deficiency (EFAD) may exist in protein–energy malnutrition (PEM). EFAD is characterised by low 18:2ω6, often in combination with low 20:4ω6 and 22:6ω3, and high 18:1ω9 and 20:3ω9. Some PEM symptoms, notably skin changes, impaired resistance to infections, impaired growth rate and disturbed development may at least partly be explained by EFAD. One or more of the following factors could induce EFAD in PEM: low EFA intake, poor lipid digestion, absorption, transport, desaturation and increased EFA β-oxidation and peroxidation. EFAD may perpetuate itself by decreasing lipid absorption and transport, and aggravate PEM by impairing nutrient absorption and dietary calorie utilisation. Micronutrient deficiencies may contribute to the impaired EFA bioavailability and metabolism. Nutritional rehabilitation strategies in PEM may consider adequate intakes of EFA and micronutrients, e.g. by promoting breastfeeding. More research is required to gain detailed insight into the role of EFAD in PEM.

Essential fatty acid deficiency (EFAD) results from low dietary intake, severe malabsorption, and/or increased physical requirements such as growth. (4) In 1971, Holman described the symptoms of EFAD in rats and other mammalian species, including primarily impaired growth and dermatitis, and secondarily steatosis, renal toxicity, pulmonary abnormalities, and increased metabolic rate. (5) In EFAD, tissue levels of both omega-3 and omega-6 fatty acids are diminished. The major biochemical changes of EFAD are decreased arachidonic acid (AA) and increased Mead acid, the latter being a downstream product of oleic acid, an omega-9 fatty acid. Desaturase enzymes display differential activity in the order of preference omega-3 > omega-6 > omega-9. Normally linoleic acid would be converted to AA, a tetraene; however in times of deficiency, de novo lipogenesis occurs, resulting the conversion of oleic acid by elongation and desaturation to Mead acid, a triene. As a result, conversion of oleic acid to Mead acid only occurs when there are low dietary levels of both ALA and LA. This metabolic switch is seen as a compensatory mechanism to maintain the number of double bonds in cell membrane fatty acids. Therefore, elevated Mead acid in conjunction with a lowered AA has been associated with EFAD.

I don't know about Choco, but imparied growth, dermatitis ( there's that pesky skin pathology again ), steatosis (fatty liver disease), renal toxicity and pulmonary abnormalities sure do sound like symptoms of a deficiency to me. And the funny thing is, all of it can be avoided by taking, GASP, toxic Cod liver oil ( you know, the equivalent of swilling WD40 in Chocos world ).

So, Choco, I'm taking you up on your offer to debunk these studies. Looking forward to sparring with you! And, by the way, I do sometimes find your advice helpful insofar as I do not put my faith in the things you say and I also do my own research!